|
|
||||||||
AJP - Endocrinology and Metabolism, Vol 257, Issue 6 E797-E803, Copyright © 1989 by American Physiological Society
ARTICLES |
Y. Takuwa, Y. Ohue, N. Takuwa and K. Yamashita
Department of Internal Medicine, University of Tsukuba, Ibaraki, Japan.
The effect of endothelin-1 (ET), a novel vasoactive peptide derived from endothelial cells, on osteoblastic MC3T3-E1 cells was studied. ET specifically binds to a single class of high-affinity receptors in MC3T3-E1 cells and induces phospholipase C activation with the production of two second messengers, inositol trisphosphate and 1,2-diacylglycerol, and a biphasic increase in intracellular free Ca2+ concentration ([Ca2+]i), which consists of an initial transient increase and an ensuing sustained plateau, as measured with a fluorescent indicator, fura-2. The second plateau phase but not the initial transient increase in [Ca2+]i induced by ET is abolished by removal of extracellular Ca2+ but not by either nicardipine, verapamil, or diltiazem. The ET-stimulated production of inositol trisphosphate is not abolished by removal of extracellular Ca2+, indicating that ET-stimulated phospholipase C activation is not a consequence of an increase in Ca2+ influx across the plasma membrane. ET causes stimulation of DNA synthesis and reduction of alkaline phosphatase activity in MC3T3-E1 cells. A protein kinase C activator phorbol 12,13-dibutyrate mimics these effects of ET. The results demonstrate that ET activates the inositol lipid signaling pathway and induces mobilization of Ca2+ from both extra- and intracellular pools and activation of protein kinase C in osteoblastic MC3T3-E1 cells.
This article has been cited by other articles:
![]() |
Y. Hiruma, A. Inoue, A. Shiohama, E. Otsuka, S. Hirose, A. Yamaguchi, and H. Hagiwara Endothelins inhibit the mineralization of osteoblastic MC3T3-E1 cells through the A-type endothelin receptor Am J Physiol Regulatory Integrative Comp Physiol, October 1, 1998; 275(4): R1099 - R1105. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |